The present invention relates to implantable medical devices, and more particularly to an implantable pulse generator and sensor, e.g., an implantable pacemaker, that senses and stimulates cardiac tissue to treat congestive heart failure (CHF).
Congestive Heart Failure (CHF) is characterized by the left, right or both ventricles losing their ability to adequately pump blood to the lungs or body. Both Systolic and Diastolic CHF may be experienced, with Systolic CHF being the more common. Systole is the contraction of the heart by which the blood is forced onward and the circulation kept up. Thus, systolic pressure is the highest arterial blood pressure of a cardiac cycle and it occurs immediately after systole of the left ventricle of the heart. In contrast, diastole is the passive rhythmical expansion or dilation of the cavities of the heart during which they fill with blood. Hence, diastolic pressure is the lowest arterial blood pressure of a cardiac cycle occurring during diastole of the heart.
The recognized medical treatment today for CHF is a pharmacological solution, e.g., Beta blockers, diuretics and/or inotropic drugs. This treatment regime does not cure the underlying substrate or eliminate the symptoms. It does, however, help mitigate the symptoms and improve the patient's quality of life on a temporary basis.
Experimental approaches for dealing with CHF in the implantable pacemaker community have focused on increasing the efficiency of the contraction by coordinating the timing between the different chambers, and on the site of stimulation within each chamber. These approaches have included, for example, the following methods individually and in parallel: (i) 3-chamber pacing; (ii) 4-chamber pacing; (iii) left ventricular pacing by a coronary sinus lead, (iv) Bachman's Bundle pacing; and (v) RVOT pacing. All have met with limited success, but all are hampered by the lack of knowledge regarding the correct dynamic timing required during the sequencing of the chambers.
Consider the manner in which the heart naturally ejects and collects blood. During systole, the heart ejects a certain volume of blood V1 into the body's arterial system. During diastole, the heart collects another volume of blood V2 returning to the heart through the body's system of veins. Assuming that the body does not loose any significant amount of blood during this ejection and collection process, the volume of ejected blood V1 should be approximately equal to the volume of collected blood V2.
However, sometimes not all of the blood held in the ventricles of the heart is ejected during systole. That is, there may be a residual volume of blood, R, that remains in the heart after blood ejection during systole. (This residual volume, R, is also referred to as the “end systolic volume”.) In the case of the left ventricle, which holds oxygen-rich blood that has returned from the lungs, any such residual volume of blood represents inefficient operation of the heart.
In the event that a residual volume of blood remains in the heart at the end of systole, when the blood returns to the heart during diastole, the volume of blood in the heart will have increased to a volume of V2+R, where V2 (the collected blood volume) is approximately equal to V1 (the ejected blood volume). The heart's natural solution to an inadequate ejection fraction (where “ejection fraction” is defined as the ejected blood volume V1 during systole divided by the total blood volume in the heart at the end of diastole, V2+R) is to make the next cardiac cycle's filling volume greater. That is, at the end of diastole, a greater volume of blood, V2+R, is in the heart, causing the heart to dilate (expand or stretch) to accommodate the increased blood volume. The increased blood volume in the heart is ejected during the next cycle, thereby providing a higher ejection fraction, and thereby self-correcting the inadequate ejection fraction. This natural self-correction is brought about by Starling's law.
Starling's law states that a muscle, including the heart muscle, responds to increased stretching at rest by an increased force of contraction when stimulated. Disadvantageously, however, there is a limit to Starling's law. That is, a point is soon reached where greater stretching does not produce a greater contraction. As a patient operates at the top of Starling's Curve, the myocardial tissue is being stretched and further dilated. This results in the growth of connective tissue within the myocardial tissue, which tissue growth hampers or hinders the muscle contraction. The stretching of the ventricles accelerates this connective tissue growth. Thus, a positive feedback loop is created moving the patient closer to a dangerous CHF situation. Additionally, the connective tissue also interferes with the conduction system of the heart, resulting in a slower, less forceful contraction. This condition may cause hyper or hypo myopathy.
Pacemakers known in the art provide monopolar or bipolar voltage stimulation, typically in the right atrium or the right ventricle. Some pacemakers and pacing leads further provide for voltage stimulation at multiple sites within the heart. See, e.g., U.S. Pat. Nos. 4,444,195; 4,848,352; 5,184,616; 5,476,502; 5,549,109; 5,800,471; 6,052,615; 6,076,014; 6,096,064; and 6,122,545.
It is a feature of the present invention to provide a more efficient and effective way to assist the heart to adequately perform its function as a pump.